Page 54 - Cardiac Nursing

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30 PA R T I / Anatomy and Physiology

Thin filament
■ Figure 1-27 In resting muscle
(right), the crossbridges project almost
at right angles to the longitudinal axis
of the thick filament. In active muscle
(left), the crossbridges interact with the
thin filaments, which are drawn to-
ward the center of the sarcomere.
(From Katz, A. [2006]. Physiology of
the heart [4th ed., p. 106]. Philadel-
Resting (Diastole) Active (Systole)
Thick filament phia: Lippincott Williams & Wilkins.)

flexing, releasing, and binding again, thus pulling the thin fila- Removal of calcium ion is essential in relaxation. Two mecha-
ment toward the center of the sarcomere in an isotonic contrac- nisms are important in this process. The SR pumps calcium ion
tion. If the muscle is held at a fixed length and is unable to shorten into its core. This is an active process and requires chemical energy
(an isometric contraction), tension is generated by the pulling of from ATP breakdown. Also, calcium ion is pumped outward
the crossbridge. across the sarcolemma. This removal process is also an active
When the muscle is relaxed during diastole, actin–myosin in- process because calcium ions must be moved against electrical and
teraction is inhibited by tropomyosin and troponin. Depolariza- concentration gradients. Rather than using ATP directly, this
tion initates inward calcium ion currents across the sarcolemma process uses the energy stored in the sodium ion gradient. In con-
and T-tubule membranes; calcium ion is then released from junction with sodium ion moving inward down its concentration
within the SR. The increased sarcoplasmic calcium ion concen- gradient, calcium ion is forced outward. The sodium ion gradient,
tration is in turn a trigger for contraction. Calcium ion binds tro- in turn, is maintained by the sodium–potassium pump, which is
ponin; tropomyosin rotates in a manner such that resting inhibi- powered by ATP.
tion to cross-bridge formation is removed, and crossbridges form The ATP required for the calcium ion removal from the sar-
(see Fig. 1-27). coplasm and for the cycling of crossbridges may be depleted, for
At relaxation, sarcoplasmic calcium ion concentration is very example, in myocardial ischemia. When this happens, cross-
low. When calcium ion concentration rises, contraction occurs. bridges form and are not broken and the muscle becomes stiff.
The sarcoplasmic calcium ion concentration determines the force-
fulness of contraction. Figure 1-30 illustrates the relationship; the Modulation of Sarcoplasmic Calcium
higher the sarcoplasmic calcium ion concentration the greater the Ion Concentration
tension the heart muscle can generate until a saturating concen-
tration is attained. Interventions that alter sarcoplasmic calcium ion concentration
alter the force generated during contraction. For example, -
Molecular Basis for Relaxation adrenergic drugs, such as epinephrine, may increase inward cal-
cium current through calcium channels opened during the action
Contraction ceases when calcium ion is removed from the sar- potential, increasing sarcoplasmic calcium ion concentration and
coplasm. Troponin releases its bound calcium ion; tropomyosin thus the force of contraction. Certain antiarrhythmic drugs such
returns to the position in which actin and myosin interaction was as procainamide are associated with decreased calcium ion release
blocked. The cell relaxes (see Fig. 1-27). from the SR and, thus, decreased systolic tension generation and
blood pressure. 55
Digitalis-like drugs increase the force of contraction. This is
possibly caused by increased sarcoplasmic calcium ion concentra-
tion. Digitalis-like drugs partially block the sodium–potassium
pump. As the transmembrane sodium ion gradient decreases, less
calcium ion is pumped out across the sarcolemma. The intracel-
lular calcium ion stores and calcium ion level during contraction
increase. The end result is augmented contractile strength.

MECHANICAL PROPERTIES OF
THE MYOCARDIUM

The heart is a pump. It functions to add energy to the flowing
blood, thus propelling the blood through the systemic and pul-
monary circulations. The performance of the heart as a pump can
■ Figure 1-28 Cross section of the thin filament in resting muscle
at the level of a troponin complex showing relationship between be described in terms of the cardiac output (CO). CO is the vol-
actin, tropomyosin, and the three components of the troponin com- ume of blood pumped by one ventricle in 1 minute. CO is equal
plex. (From Katz, A. [2006]. Physiology of the heart [4th ed., p. 110]. to the stroke volume (SV), or volume of blood pumped with each
Philadelphia: Lippincott Williams & Wilkins.) beat times the number of cardiac contractions (heart rate, HR) in